Biomedical subjects
Publications and source records attributed to J Lory.
This article summarizes aspects of diagnosis and treatment, resources and administrative organization of the geriatric day hospital of the Spital Bern--Ziegler.
The contribution of cell-mediated cytotoxicity to the pathogenesis of inflammatory bowel disease (IBD) is controversial, and results of in vitro assays vary according to experimental procedures. Therefore, we compared the frequency of cytotoxic effector cells in situ. On tissue sections of controls (n = 11), low frequencies of granzyme A and perforin mRNA-expressing cells are found in the lamina propria (1.77 +/- 0.15% and 1.46 +/- 0.12%, respectively) and in the epithelial cell layer (0.76 +/- 0.12% and 0.66 +/- 0.10%, respectively). In patients with IBD (n = 33), corresponding values were significantly (P < 0.02) higher, 6.1 +/- 0.40% and 5.92 +/- 0.57% for granzyme A and perforin expression in the lamina propria and 2.50 +/- 0.19% and 2.59 +/- 0.28%, respectively, in the epithelial compartment. Differences between ulcerative colitis and Crohn's disease are statistically not significant (P > 0.33). Activated cytotoxic cells are preferentially found at sites facing the intestinal lumen. Perforin mRNA-expressing cells are mainly CD8+ T cells. CD4+ T cells expressing perforin mRNA are mainly isolated from affected areas of patients with Crohn's disease. Immunostaining for perforin protein generally coincides with perforin mRNA in situ. These data demonstrate that cytotoxic cells are vigorously activated in situ in the intestinal mucosa of patients with active IBD.
Liver biopsies in hepatitis C frequently show bile duct damage, lymphoid follicles, large and small droplet fat, hepatocyte multinucleation. Mallory body-like material, and activation of sinusoidal inflammatory cells. Even though these lesions are useful parameters in the diagnosis of hepatitis C, their specificity remains uncertain. Endotheliitis-like changes of small portal veins have been described for various liver diseases, including viral hepatitis. The aim of the present study was to investigate the prevalence and severity of endotheliitis-like changes in chronic hepatitis C in comparison with chronic hepatitis B. For this purpose, liver biopsies of 50 patients with chronic hepatitis C and 48 patients which chronic hepatitis B were systematically analyzed for the presence of endotheliitis-like changes. Endotheliitis-like changes were defined as lymphocytic infiltration of venous walls, subendothelial lymphocyte accumulation, adherence of lymphocytes to the endothelium, and endothelial cell damage. Endotheliitis-like change severity was graded (borderline/questionable; slight to moderate; severe), and endotheliitis-like changes were analyzed in small portal veins and in central veins. Endotheliitis-like changes were significantly more frequent in chronic hepatitis C than in chronic hepatitis B (41.5% vs. 6.9%; p < 0.05). In chronic hepatitis C, endotheliitis-like changes predominated in small portal veins, but 27% of small hepatic veins were involved as well. The findings indicate that endotheliitis-like changes may represent a useful histological parameter in the diagnosis of chronic hepatitis C.
The term, atrophy/hypertrophy complex (AHC) of the liver, denotes a distinct combination of hepatic atrophy and hypertrophy occurring in situations of significant impairment of bile flow and/or portal or hepatic venous blood flow. In the lobes or segments concerned atrophy ensues, whereas areas not or less involved develop compensatory hypertrophy, resulting in a characteristic gross deformity of the organ and, in some instances, in rotation of the liver around a virtual hilar axis. As recognition and early detection of AHC have a strong implication on the treatment of several hepatobiliary diseases, adequate combined clinical, radiological and histopathological strategies have to be used in order to arrive at a correct diagnosis. The present investigation was designed to analyze the morphology of AHC in detail and to define lesion patterns having the highest predictive value. For atrophy, the following features were highly characteristic: 1) Advanced septal fibrosis with or without nodular change of parenchyma; 2) Biliary piecemeal necrosis with formation of vascular structures; 3) Ductular proliferations, frequently extending into septa and involving the parenchyma; 4) Capillarization of sinusoids with type IV collagen deposition in Disse's space; 5) Factor VIII-associated antigen expression by sinusoidal endothelia; 6) a seemingly paradoxical increase of proliferative activity of hepatocytes as based on PCNA staining. The severity of lesions in atrophy was related to the type of underlying disease, in that the changes were clearly more expressed in situations of longstanding obstruction due to benign disease. Using a set of well-defined morphological parameters, atrophy can be reproducibly distinguished from hypertrophy in biopsy material from AHC.